Diabetes is now one of the most common chronic diseases in China, and incidences of diabetes in youth have been on the increase. Complications resulting from long-term poorly controlled diabetes can affect many organs throughout the body, including the nervous system. Recent studies have found that various neurological diseases complicated with diabetes can be improved with the use of glucagon-like peptide-1 receptor agonists (GLP-1RA) for the treatment of diabetes, but the exact mechanism is not fully understood. GLP-1 receptor is a transmembrane G protein-coupled receptor found in pancreatic cells and vascular endothelium. Natural GLP-1 is an intestinal peptide-like hormone secreted by feeding-induced stimulation of L cells in the ileum and colon, and it promotes insulin synthesis and secretion. A variety of long-acting GLP-1RA developed to overcome the short half-life of GLP-1 have been widely used in clinical practice, such as exenatide, liraglutide, albiglutide, and dulaglutide, which have shown advantages in controlling blood glucose levels and body weight. Since of GLP-1 receptors are widely distributed on the cell membranes of tissues such as the pancreas, lung, brain, heart, kidney and gastrointestinal tract, GLP-1RA may have a wider application other than the treatment of diabetes. Existing reports have shown that GLP-1RA also has significant function in neurological, cardiovascular, and renal protective effects, as well as other effects such as anti-respiratory inflammation and fat reduction. GLP-1 receptors are also widely distributed in the brain, and GLP-1 and its analogs can cross the blood-brain barrier, thus affecting central nervous system function. This paper analyzed the possible mechanisms of GLP-1RA neuroprotection in various neurological diseases such as ischemic stroke, cognitive dysfunction, and Parkinson's disease and other neurological diseases. When GLP-1RA is applied to ischemic stroke disease, previous studies have found that GLP-1RA binds to the corresponding receptors to activate multiple kinase signaling pathways such as PKA, PI3K/AKT, ERK, MEK, etc., to regulate neurotransmitter transmission and achieve results such as anti-inflammation, reduction of oxidative stress, inhibition of apoptosis, and reduction of DNA damage. In terms of cognitive disorders, many literatures have confirmed that the improvement of cognition by GLP-1RA may be related to its modulation of neurotransmitter transmission in brain domains associated with cognitive function, and subsequently promotes neuroprotection through various pathophysiological mechanisms such as anti-inflammation, anti-apoptosis, autophagy, modulation of insulin signaling pathways, reduction of cytotoxicity, and reduction of aggregation and deposition of β-amyloid and Tau proteins. In the context of Parkinson's disease, GPL-1RA has turned out to have the function of protect motor activity and dopaminergic neurons in animal models of Parkinson's disease. GPL-1RA can also be used to reduce oxidative stress, inflammation, reduce dopaminergic neuron loss, promote growth factor expression, and also improve tyrosine hydroxylase expression in experimental animals. Previous researches on GPL-1RA are not only limited to basic experiments, clinical studies have also demonstrated its therapeutic efficacy in a variety of neurological diseases. Therefore, this article will describe the research progress of GLP-1 receptor agonists in neuroprotection in various neurological diseases such as cerebral infarction, cognitive dysfunction, and Parkinson's disease, in order to summarize their mechanism of action and discuss their potential as neuroprotective drugs.